癌症研究
白血病
生物
干细胞
转录因子
癌症
癌基因
T细胞白血病
癌症干细胞
细胞
利基
免疫学
细胞生物学
遗传学
基因
细胞周期
生态学
作者
David J. Curtis,Matthew P. McCormack
标识
DOI:10.1158/1078-0432.ccr-10-0440
摘要
T-cell acute lymphoblastic leukemia (T-ALL) is commonly caused by the overexpression of oncogenic transcription factors in developing T cells. In a mouse model of one such oncogene, LMO2, the cellular effect is to induce self-renewal of committed T cells in the thymus, which persist long-term while acquiring additional mutations and eventually giving rise to leukemia. These precancerous stem cells (pre-CSC) are intrinsically resistant to radiotherapy, implying that they may be refractory to conventional cancer therapies. However, they depend on an aberrantly expressed stem cell-like self-renewal program for their maintenance, in addition to a specialized thymic microenvironmental niche. Here, we discuss potential approaches for targeting pre-CSCs in T-ALL by using therapies directed at oncogenic transcription factors themselves, downstream self-renewal pathways, and the supportive cell niche.
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